Uric Acid Test

Your body is constantly breaking down and recycling old cells. One of the leftovers from that process is uric acid, a molecule that builds up in your blood when production outpaces your kidneys' ability to flush it out. When levels climb too high, uric acid can crystallize in your joints, damage your kidneys, and drive up your risk of heart disease, stroke, and high blood pressure. When levels drop too low, you may lose a layer of antioxidant protection that your blood normally provides.

What makes this test especially useful for someone focused on prevention is that uric acid doesn't show up on standard blood panels. Neither the basic metabolic panel nor the comprehensive metabolic panel includes it. That means your level could be quietly elevated for years without anyone noticing, even if you're getting regular lab work.

What Uric Acid Is and Where It Comes From

Uric acid is the final breakdown product of molecules called purines, which are the building blocks of DNA and RNA in every cell. When cells die and get recycled (a normal, constant process), the purines inside them are converted into uric acid, mainly by an enzyme called xanthine oxidase that operates in your liver, intestines, and blood vessel walls. A smaller share of your uric acid comes from purine-rich foods like red meat, organ meats, shellfish, and beer.

About two-thirds of the uric acid your body makes is eliminated through the kidneys, and the remaining third exits through the gut. Your kidneys filter uric acid, then reabsorb most of it back into the blood. Only about 8 to 12% of the filtered uric acid actually leaves your body in urine. This means your serum uric acid level reflects a balance between how much your body produces and how efficiently your kidneys clear it.

Gout: When Crystals Form

The most well-known consequence of high uric acid is gout, a form of arthritis caused by needle-shaped crystals of a salt called monosodium urate depositing in joints and surrounding tissues. Uric acid starts to crystallize when blood levels exceed approximately 6.8 mg/dL, which is the saturation point at normal body temperature and pH. These crystals trigger intense inflammatory attacks, most commonly in the big toe, but also in ankles, knees, wrists, and elbows.

Not everyone with elevated uric acid develops gout. In one long-term study, most people with levels above 10 mg/dL still hadn't developed gout after 15 years. But crystal deposits can form silently in joints for years before the first painful flare. Once gout is established, the treatment target is to bring uric acid below 6 mg/dL (and below 5 mg/dL in severe cases) to dissolve existing crystals and prevent new ones from forming.

Kidney Disease

Elevated uric acid is independently linked to the development and progression of chronic kidney disease (CKD). A meta-analysis of 15 cohort studies covering about 99,000 people found that for every 1 mg/dL increase in uric acid, the risk of developing CKD rose by 22%. A larger pooled analysis of 30 cohort studies confirmed this, showing a 15% increase in CKD risk per 1 mg/dL increment. The association was stronger in people under age 60.

This creates a vicious cycle: kidney disease raises uric acid (because the kidneys can't clear it as well), and high uric acid may accelerate further kidney damage. If you already have reduced kidney function, monitoring uric acid is especially relevant. About one-third of people with CKD also have gout, yet fewer than one in four achieve target uric acid levels with treatment.

Heart Disease and Stroke

The cardiovascular risks of high uric acid extend well beyond gout. A 2025 meta-analysis of over 1 million participants found that hyperuricemia was associated with a 21% higher risk of coronary heart disease, a 20% higher risk of dying from coronary heart disease, and a 75% higher risk of cardiovascular death. For every 1 mg/dL increase, the risks of coronary heart disease, coronary death, and cardiovascular death rose by 16%, 13%, and 11%, respectively.

Sources: Lyu et al. 2025 meta-analysis; Li et al. 2016 meta-analysis; Qiao et al. 2021 meta-analysis.

What this means for you: the association between uric acid and cardiovascular events is consistent across large studies and persists after adjusting for standard risk factors like blood pressure, cholesterol, BMI, and diabetes. The risk appears to be particularly strong in women, especially after menopause. Whether directly lowering uric acid with medication reduces heart attack or stroke risk in people without gout remains unproven, but knowing your level helps you understand your overall cardiometabolic picture.

High Blood Pressure

Hyperuricemia may also set the stage for high blood pressure. A meta-analysis of 25 studies covering about 98,000 people found that those with hyperuricemia had roughly 48% higher odds of developing hypertension, and each 1 mg/dL increase raised the risk by 15%. This dose-response relationship held after adjusting for other risk factors.

The URRAH study, which followed over 22,000 people, identified uric acid thresholds that predicted mortality that were considerably lower than traditional hyperuricemia cutoffs: 4.7 mg/dL for total mortality and 5.6 mg/dL for cardiovascular mortality. These findings suggest that the risk begins rising at levels many labs would still label as "normal."

Heart Failure

A meta-analysis of studies on new-onset heart failure found that people with hyperuricemia had about 65% higher risk of developing heart failure. For every 1 mg/dL increase in uric acid, the odds of heart failure rose by 19%. In a separate study of over 18,000 adults who already had cardiovascular disease, those in the highest uric acid group had 50% greater risk of developing heart failure compared to those in the lowest group.

The J-Shaped Curve: Too Low Can Be a Problem Too

Uric acid has antioxidant properties in the blood, and very low levels may indicate their own set of concerns. A Japanese nationwide cohort of over 500,000 people found a J-shaped relationship with mortality: risk increased at levels above 7 mg/dL in men and 5 mg/dL in women, but also at very low levels. A Korean cohort study confirmed this U-shaped pattern, with increased mortality at both extremes.

Low uric acid (below about 2 mg/dL) can sometimes signal inherited kidney transport defects, problems with the proximal tubules in the kidney, or severe nutritional deficiency. If your level is unusually low, it deserves the same attention as an unusually high one.

Sex, Age, and Ethnic Differences

Uric acid levels differ markedly between men and women, and these differences shift with age. Men average about 5.3 mg/dL and women about 4.1 mg/dL in large population studies. In men, levels rise gradually, about 0.1 mg/dL per decade. In women, levels stay relatively stable until menopause (around age 50), then climb sharply, about 0.4 mg/dL per decade. By age 65, the prevalence of hyperuricemia in women exceeds that of men.

Ethnicity also plays a role. In a large U.S. analysis, non-Hispanic Black adults had the highest hyperuricemia prevalence (about 24% in both sexes), and a separate study found that Black women had over twice the risk of developing hyperuricemia compared to white women over follow-up, despite starting with lower baseline levels.

Reference Ranges

Traditional lab reference ranges are based on what is statistically common in the population, not on what is physiologically safe. Many labs report the upper limit of normal as 7.0 to 7.2 mg/dL for men, which is above the crystallization threshold of 6.8 mg/dL. That means a lab could call your result "normal" while crystals are already capable of forming in your joints. Kidney function, sex, age, BMI, and medications all influence where your level sits, so these ranges should be interpreted alongside your full clinical picture.

These tiers are drawn from published research, including the URRAH study, the Japanese 5-year cohort, and the Irish cohort study. Your lab may use different assays and cutpoints. Compare your results within the same lab over time for the most meaningful trend.

Tracking Your Trend

A single uric acid reading gives you a useful snapshot, but tracking your level over time tells a much richer story. Uric acid has a within-person biological variation of about 5 to 7%, meaning your true level can naturally fluctuate by that much from one draw to the next, even when nothing has changed. Because of this, a meaningful change between two readings needs to exceed roughly 15 to 20% to be confident it reflects a real biological shift rather than normal variation.

Measurements taken years apart correlate strongly (r = 0.81), which means your general level is fairly stable over time. But if you're making dietary changes, losing weight, starting a new medication, or taking supplements that affect purine metabolism, retesting in 3 to 6 months lets you see whether those changes are actually moving your number. After that, annual monitoring is reasonable for most people. If you're on urate-lowering medication, periodic testing (at least once or twice a year once stable) helps confirm you're staying at target.

One important nuance: a study of over 3,000 adults found that repeat testing did not meaningfully improve the ability to predict who would develop gout compared to a single measurement. The predictive accuracy was essentially the same whether researchers used one reading, two readings, or the average. This suggests that for risk assessment purposes, a single reading is informative. But for monitoring an intervention, tracking your trend remains valuable.

When Results Can Be Misleading

Uric acid levels can shift substantially based on factors that have nothing to do with your long-term health status. The most common sources of misleading readings:

• Time of day: Morning levels can be up to 30% higher than afternoon levels. If you draw blood at 8 AM one time and 5 PM the next, you might see a large apparent change that's just circadian rhythm. Stick to the same time of day for each draw.
• Fasting and ketosis: Prolonged fasting dramatically raises uric acid. In one study, levels more than doubled (from 5.9 to 12.5 mg/dL) after 7 days of fasting, because ketones produced during fasting compete with uric acid for excretion through the kidneys. Even overnight fasts of 14 hours or more are associated with modestly higher levels.
• Intense exercise: A single bout of high-intensity exercise (such as sprinting or heavy lifting) can acutely raise uric acid by about 40% through the breakdown of energy-carrying molecules in muscle. This effect can persist for 24 to 48 hours. Moderate, sustained exercise does not produce this spike. Avoid intense workouts the day before testing.
• Acute illness or surgery: Inflammation from illness or surgery can temporarily lower uric acid by about 10 to 15% for 48 to 72 hours. During an acute gout flare, uric acid often drops paradoxically, which can fool both you and your doctor into thinking levels are normal when they're not.

Several common medications can also shift your reading without affecting your underlying gout or cardiovascular risk. Corticosteroids like prednisone at high doses (60 mg/day) can lower uric acid by about 3 mg/dL by increasing kidney clearance, not by fixing an underlying problem. High-dose propranolol and certain other beta-blockers can raise levels. Thiazide and loop diuretics (commonly prescribed for blood pressure) significantly increase uric acid through multiple kidney mechanisms. If you're taking any of these, your doctor should factor the medication effect into the interpretation.